We hypothesize that skin microbiota (bacteria, fungi, viruses, phage, archae) plays a role in common dermatological conditions, such as atopic dermatitis (eczema). There are two classical explanations for the role microbes play in skin disease: (1) a specific microbe colonizes the skin to disrupt the balance of commensal microflora, or (2) microbes release toxic substances or invade cells to induce an inflammatory response directly. Since culture-dependent skin sampling methods are incomplete, biased assessments of microbial diversity, we propose to use genomic methods to sample skin microflora and shed light on the above conjectures. A cultivation-independent genomic approach directly sequences the microbial DNA, enabling us to imply microbial community membership, structure and diversity. Our initial study of skin bacteria analyzed the bacterial 16s rRNA gene, which contains highly conserved regions, allowing for amplification with specific primers, that flank highly variable regions. These sequences suggest the identity of the species being sampled and enable us to infer phylogenetic relationships. This work has implications for psoriasis and atopic dermatitis (eczema), with long term significance for asthma and hay fever. We also utilize genomics to study emerging pathogens in the clinical center. For example, we performed whole-genome shotgun sequencing of three isolates from an outbreak of Acinetobacter baumannii at the NIH Clinical Center in 2007.